الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Summary and conclusion
In this work, the role of protein kinase c in diabetic macrovascular dysfunction was studied.
Initially we induced two experimental models; diabetic model (by streptozotocin injection) and insulin resistance (by fructose administration). Both of which were accompanied with vascular complications.
The vascular complications associated with two experimental models (diabetes and insulin resistance) were fully investigated; the systolic and diastolic blood pressures were recorded. Vascular reactivity to standard vasoconstrictors; phenylephrine and KCl and vasodilators; acetylcholine and sodium nitroprusside were examined using the isolated artery technique. Serum level of glucose, insulin, triglycerides, total cholesterol, tumer necrosis factor and advanced glycation end products were also determined in addition to arginase activity.
In order to explain the mechanism of endothelial dysfunction associated with diabetes and insulin resistance, the basal vascular level of reactive oxygen species was determined.
In addition, the acute effect of protein kinase c inhibition by in vitro incubation with chelerythrine on vascular dysfunction in diabetes or insulin resistance was also examined by incubating aorta isolated from diabetic or insulin resistance animals with protein kinase c inhibitors then the vascular reactivity was studied.
To confirm the role of protein kinase c enzyme in the seen vascular dysfunction, aorta isolated from normal animals were incubated with protein kinase c stimulant, Phorbol 12-myristate 13-acetate, with or without protein kinase c inhibitors and then the vascular reactivity was examined using the isolated artery technique.
Finally the acute effect of in vitro incubation with apigenin, a natural flavonoid with PKC inhibiting activity, on the vascular reactivity was examined using the isolated artery technique on aorta isolated from diabetic, IR or normal animals (incubated with PMA).